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S Linthicum

Publications and source records attributed to S Linthicum.

4 recordsLinked to original sources
PubMed1999

pH dependence of antibody: hapten association.

Monoclonal antibody NC6.8 is specific for the superpotent sweetener, N-(p-cyanophenyl)-N'-(diphenylmethyl)-guanidiniumacetic++ + acid. The three-dimensional structure of the complex shows the close proximity of complementary charged residues on the antibody and groups of the hapten. As a result, association is dependent on the pH, dielectric, and ionic strength of the medium. Continuum electrostatics methods are used to calculate the pH-dependent association energetics of NC6.8 with the superpotent sweetener. In addition to providing a titration profile, the calculations quantitatively assess the relative influence of charged groups on the energetics of association. Models of site directed mutants are constructed to probe the influence of each charged interface residue on the pH-dependent energetics of association. Examination of electrostatic contribution to free energy of association in mutant complexes, where the key acidic residues on the antibody are neutralized, shows that charge complementarity at the combining site is an important requirement for hapten binding. Also, based on the pKa values of several combining site tyrosine residues, aromatic pi-stacking and van der Waal's contacts between the antibody and hapten contribute to the specificity of the complex.

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PubMed1993

Correlation between susceptibility to demyelination and interferon-gamma induction of major histocompatibility complex class II antigens on murine cerebrovascular endothelial cells.

The induction of major histocompatibility complex (MHC) Class II expression was studied on cerebrovascular endothelial cells (CVE) obtained from strains of mice that are resistant (BALB/c) and susceptible (SJL and CBA) to Theiler's virus-induced demyelination (TVID). Following 24 h treatment with interferon (IFN)-gamma, MHC Class II was induced on CVE derived from susceptible but not resistant strains of mice. However, IFN-gamma induced the expression of MHC Class II on late passages of BALB/c CVE. These results demonstrate a correlation between susceptibility to demyelination and the ability of IFN-gamma to induce the expression of MHC Class II on CVE. In susceptible strains of mice, the presence of activated, IFN-gamma-secreting T cells, in the vicinity of CVE would increase the antigen-presenting capabilities of CVE and result in increased T cell traffic into the central nervous system.

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